Hanyang University Hospital for Rheumatic Diseases, Seoul, Republic of Korea.
Immunol Lett. 2013 Jul-Aug;154(1-2):80-5. doi: 10.1016/j.imlet.2013.08.012. Epub 2013 Sep 5.
Triggering receptor expressed on myeloid cells-1 (TREM-1) is a recently identified cell surface receptor that is expressed mainly on monocytes and neutrophils, and acts as an amplifier of immune responses. In this study, 1,25(OH)2D3 strongly upregulated the expression of TREM-1 in human monocytes and macrophages. 1,25(OH)2D3 stimulated TREM-1 mRNA expression by augmenting transcription, and not by inhibiting mRNA degradation. The upregulated expression of TREM-1 by 1,25(OH)2D3 was dependent on the NF-κB signaling pathway and required new protein synthesis in differentiated U937 macrophages. Our results show that 1,25(OH)2D3 can affect the innate and inflammatory responses by upregulating TREM-1 expression, and suggest that 1,25(OH)2D3 may function as an enhancer of the innate immune response by upregulating TREM-1 expression, in addition to inducing the antimicrobial peptide cathelicidin.
髓系细胞触发受体-1（TREM-1）是一种新发现的细胞表面受体，主要表达于单核细胞和中性粒细胞上，并作为免疫反应的放大器。在本研究中，1,25(OH)2D3 可强烈上调人单核细胞和巨噬细胞中 TREM-1 的表达。1,25(OH)2D3 通过增强转录而不是抑制 mRNA 降解来刺激 TREM-1 mRNA 的表达。1,25(OH)2D3 上调 TREM-1 的表达依赖于 NF-κB 信号通路，并需要分化的 U937 巨噬细胞中的新蛋白质合成。我们的结果表明，1,25(OH)2D3 可以通过上调 TREM-1 的表达来影响先天和炎症反应，提示 1,25(OH)2D3 除了诱导抗菌肽 cathelicidin 外，还可以通过上调 TREM-1 的表达来增强先天免疫反应。
